Angiotensin II is the most active vasoconstrictor agent and acts to control the rate of secretion of aldosterone by the adrenal cortex. Therefore, angiotensin II can alter blood pressure both by its effect on vascular reactivity and through its effect on sodium and extracellular fluid volume. Furthermore, it can alter its rate of formation by directly suppressing renin release by the kidney. Thus, comparative studies of the characteristics of the receptors for angitotensin II on vascular smooth muscle, the juxtaglomerular apparatus and the glomerulosa cell may be of critical importance in evaluating the role of altered agonist receptor relationship in disease states. In addition to angiotensin II, glomerulosa and juxtaglomerual tissue are responsive to a variety agents some of which may also influence the tissue's response to angiotensin II. The proposed research program has the following objectives. The first is to characterize the receptors for angiotensin II on vascular, adrenal and renal tissue by two or more techniques; classical binding studies, pharmacologic structure-activity relationships, and binding response studies. Thus, the studies will be performed on isolated cell suspension which have been purified either by unit gravity sedimentation or receptor affinity chromatography techniques. The cell suspensions will contain only glomerulosa or juxtaglomerula cells. Finally, the purified cell suspensions will be used to assess the relationship of several factors controlling aldosterone and renin release. Specifically, the relationship between the macula densa cell, sodium, catecholamines and the juxtaglomerula cell in regulating renin release will be evaluated. These studies should provide important new information about the role of angiotensin in normal sodium homeostasis and the maintenance of blood pressure. Definition of these normal control mechanisms could then logically lead to studies of the pathogenesis of certain hypertensive and edematous disorders.